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A mechanistic classification of clinical phenotypes in neuroblastoma (TERT expression threshold cohort)

ABSTRACT: A mechanistic classification of clinical phenotypes in neuroblastoma (TERT expression threshold cohort)

PROVIDER: PRJNA493609 | ENA |

REPOSITORIES: ENA

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A mechanistic classification of clinical phenotypes in neuroblastoma (TERT expression threshold cohort)

Project description:Our study proposes a precise mechanistic classification of clinical neuroblastoma phenotypes that is based on telomere maintenance mechanisms and RAS or p53 pathway mutations. A crucial factor in telomere maintenance is overexpression of TERT. We therefore determined a TERT expression threshold to identify MYCNWT TERTWT tumors whose TERT mRNA levels are comparable to those of tumors bearing MYCN or TERT alterations.

2018-10-25 | GSE120568 | GEO

A mechanistic classification of clinical phenotypes in neuroblastoma (telomere maintenance cohort)

Project description:Our study proposes a precise mechanistic classification of clinical neuroblastoma phenotypes that is based on telomere maintenance mechanisms and RAS or p53 pathway mutations. A crucial factor in telomere maintenance is overexpression of TERT. We therefore determined a TERT expression threshold to identify MYCN-WT TERT-WT tumors whose TERT mRNA levels are comparable to those of tumors bearing MYCN or TERT alterations.

2018-10-25 | GSE120559 | GEO

A mechanistic classification of clinical phenotypes in neuroblastoma (telomere maintenance cohort)

Project description:A mechanistic classification of clinical phenotypes in neuroblastoma (telomere maintenance cohort)

| PRJNA493570 | ENA

A mechanistic classification of clinical phenotypes in neuroblastoma

Project description:A mechanistic classification of clinical phenotypes in neuroblastoma

| PRJNA493612 | ENA

Contribution of DNA methylation profiling in the classification of TRIO::TERT sarcomas

Project description:DNA methylation profiling has emerged as a valuable tool for tumor classification, exemplified by the German Cancer Research Center's creation of online classifiers for CNS tumors and sarcomas. Identification of rare molecular events, such as TRIO::TERT fusion in undifferentiated sarcomas, through DNA methylation profiling and transcriptome analysis aims to define distinct molecular subgroups within sarcomas of uncertain diagnosis, potentially improving classification and treatment strategies.In this study, we present 8 cases of sarcomas characterized by TRIO::TERT fusion, establishing it as a distinct molecular subtype of sarcomas. This fusion represents a consistent molecular feature across all analyzed tumors, suggesting its pivotal role in sarcomatogenesis. Identifying TRIO::TERT transcript sarcoma as a new tumor type may enhance diagnostic strategies for improved patient management.

2024-05-31 | GSE261891 | GEO

Contribution of DNA methylation profiling in the classification of TRIO::TERT sarcomas

Project description:Contribution of DNA methylation profiling in the classification of TRIO::TERT sarcomas

| PRJNA1089517 | ENA

A mechanistic classification of clinical phenotypes in neuroblastoma

Project description:Clinical courses of the pediatric tumor neuroblastoma range from fatal progression to spontaneous regression. To gain insights into the pathogenesis of these divergent subtypes, we performed massively parallel sequencing of 416 pretreatment neuroblastomas and assessed telomere maintenance mechanisms in 208/416 cases. We observed that telomere maintenance and mutations in RAS or p53 pathway genes strongly affected disease courses. Fatal outcome occurred only in the presence of telomere maintenance, whereas patients whose tumors lacked such mechanisms had excellent outcome. In patients with telomere maintenance-positive tumors, survival was dramatically inferior when additional RAS/p53 pathway mutations were present. By contrast, spontaneous regression occurred both in the presence and absence of RAS/p53 pathway mutations in patients with telomere maintenance-negative tumors. Together, our data provide a precise mechanistic classification of clinical neuroblastoma phenotypes based on telomere maintenance mechanisms and genetic alterations of the tumor.

| EGAS00001003244 | EGA

Sequencing of Danio rerio skin from wildtype and two tert mutant phenotypes (JenAge)

Project description:Comparison of gene expression profiles from Danio rerio skin of wiltype (AB) and homozygote/heterozygote tert mutant phenotypes (AB tert(-/-), AB tert(+/)). The RNA-seq data comprises 3 groups. Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de)

2021-10-19 | GSE102434 | GEO

A mechanistic classification of clinical phenotypes in neuroblastoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-10-25 | GSE120572 | GEO

PITX1 suppresses TERT transcription

Project description:Using microcell-mediated chromosome transfer (MMCT) into the mouse melanoma cell line, B16F10, we have previously found that human chromosome 5 carries a gene, or genes, that can negatively regulate TERT expression. To identify the gene responsible for the regulation of TERT transcription, we performed cDNA microarray analysis using parental B16F10 cells, telomerase negative B16F10 microcell hybrids with a human chromosome 5 (B16F10MH5), and its revertant clones (MH5R) with reactivated telomerase. Here we report the identification of PITX1, whose restoration leads to the downregulation of mouse tert (mtert) transcription, as a TERT suppressor gene. Additionally, both human TERT (hTERT) and mouse TERT (mtert) promoter activity can be suppressed by PITX1. We showed that three and one binding sites, respectively, within the hTERT and mtert promoters that express a unique conserved region are responsible for the transcriptional activation of TERT. Furthermore, we showed that PITX1 binds to the TERT promoter both in vitro and in vivo. Thus, PITX1 suppresses TERT transcription through direct binding to the TERT promoter, which ultimately regulates telomerase activity.

2010-09-10 | GSE23216 | GEO

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